Type I Hypersensitivity (Allergic)

In Type I Hypersensitivity, an antigen is presented to CD4+ TH2 cells specific to the antigen that stimulate B-cell production of
IgE antibodies also specific to the antigen. The difference between a normal infectious immune response and a type 1
hypersensitivity response is that in type 1 hypersensitivity the antibody is IgE instead of IgA, IgG, or IgM. During sensitisation,
the IgE antibodies bind to Fc receptors on the surface of tissue mast cells and blood basophils. Mast cells and basophils coated by
IgE antibodies are "sensitised." Later exposure to the same allergen cross-links the bound IgE on sensitised cells, resulting in
degranulation and the secretion of pharmacologically active mediators such as histamine, leukotriene (LTC4 and LTD4), and
prostaglandin that act on the surrounding tissues. The principal effects of these products are vasodilation and smooth-muscle
contraction.
- Allergy
Type II Hypersensitivity (Cytotoxic)
In Type II Hypersensitivity (or cytotoxic hypersensitivity), the antibodies produced by the immune response bind to antigens on
the patient's own cell surfaces. The antigens recognized in this way may either be intrinsic ("self" antigen, innately part of the
patient's cells) or extrinsic (adsorbed onto the cells during exposure to some foreign antigen, possibly as part of infection with a
pathogen). These cells are recognized by macrophages or dendritic cells, which act as antigen-presenting cells. This causes a B
cell response, wherein antibodies are produced against the foreign antigen.
- Myasthenia Gravis (Nicotinic ACh receptors)
- Graves disease (TSH receptors)
- Rheumatic Fever (antigen on heart tissue similar to Group A -Haemolytic Streptococci cross-reactivity)
Type III Hypersensitivity (Immune complex deposition)
Type III hypersensitivity occurs when there is an excess of antigen, leading to small immune complexes being formed that do not
fix complement and are not cleared from the circulation. It is characterized by solvent antigens that are not bound to cell surfaces
(which is the case in type II hypersensitivity). When these antigens bind antibodies, immune complexes of different sizes form.
Large complexes can be cleared by macrophages but macrophages have difficulty in the disposal of small immune complexes.
These immune complexes insert themselves into small blood vessels, joints, and glomeruli, causing symptoms. Unlike the free
variant, a small immune complex bound to sites of deposition (like blood vessel walls) are far more capable of interacting with
complement; these medium-sized complexes, formed in the slight excess of antigen, are viewed as being highly pathogenic. Such
depositions in tissues often induce an inflammatory response, and can cause damage wherever they precipitate. The cause of
damage is as a result of the action of cleaved complement anaphylotoxins C3a and C5a, which, respectively, mediate the induction
of granule release from mast cells (from which histamine can cause urticaria), and recruitment of inflammatory cells into the
tissue (mainly those with lysosomal action, leading to tissue damage through frustrated phagocytosis by PMNs and macrophages).
Type IV Hypersensitivity (Delayed)
CD4+ helper T cells recognize antigen in a complex with MHC Class 2. The antigen-presenting cells in this case are macrophages
that secrete IL-12, which stimulates the proliferation of further CD4+ TH1 cells. CD4+ T cells secrete IL-2 and interferon gamma,
further inducing the release of other T H1 cytokines, thus mediating the immune response. Activated CD8 + T cells destroy target
cells on contact, whereas activated macrophages produce hydrolytic enzymes and, on presentation with certain intracellular
pathogens, transform into multinucleated giant cells.
- Type I Diabetes Mellitus
- Rheumatoid Arthritis
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